The burden of hepatitis B virus (HBV) disease and efforts to control infection will determine the future size of the population requiring treatment of HBV infection. To quantify the current prevalence of HBV infection and to reexamine the epidemiology of HBV infection, a structured review was conducted that focused on available primary literature for over 30 countries worldwide. The prevalence of chronic HBV infection continues to be highly variable, ranging over 10% in some Asian and Western Pacific countries to under 0.5% in the United States and northern European countries. The current global estimate of the number of HBV infected individuals is 350 million. Routes of transmission include vertical (mother to child or generation to generation through close contact and sanitary habits), early life horizontal transmission (through bites, lesions, and sanitary habits), and adult horizontal transmission (through sexual contact, intravenous drug use, and medical procedure exposure) and are evident to varying degrees in every country. Younger age at acquisition of infection continues to be the most important predictor of chronic carriage. However, the choice of serologic markers, temporal influences, and representativeness of the study population limit comparability of HBV seroprevalence results. HBV vaccination programs will decrease the future global burden of HBV infection and evidence of reduced burden is mounting in country-specific populations, but vaccination programs have still not been implemented in all countries, thereby maintaining reservoirs of infection and continued HBV transmission. Regardless of vaccination, large numbers of persons are infected with HBVor will become infected. Preventing the most severe HBV disease consequences in infected individuals, such as cirrhosis and hepatocellular carcinoma, will require appropriate therapeutic agents.
From the *Pharmaceutical Outcomes Research and Policy Program and §Division of Gastroenterology and Hepatology, University of Washington, Seattle, WA; †Blood Systems Research Institute, San Francisco, CA; and ‡Pharmaceutical Research Institute, Bristol-Myers Squibb, Wallingford, CT.
Received for publication June 30, 2004; accepted August 4, 2004.
Supported by a grant from the Pharmaceutical Research Institute, Bristol-Myers Squibb Company.
Reprints: Brian Custer, MPH, PhD, Blood Systems Research Institute, 270 Masonic Avenue, San Francisco, CA 94118 (e-mail: firstname.lastname@example.org).